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Publication : Focal adhesion kinase modulates activation of NF-kappaB by flow in endothelial cells.

First Author  Petzold T Year  2009
Journal  Am J Physiol Cell Physiol Volume  297
Issue  4 Pages  C814-22
PubMed ID  19587216 Mgi Jnum  J:154139
Mgi Id  MGI:4367323 Doi  10.1152/ajpcell.00226.2009
Citation  Petzold T, et al. (2009) Focal adhesion kinase modulates activation of NF-kappaB by flow in endothelial cells. Am J Physiol Cell Physiol 297(4):C814-22
abstractText  Atherogenesis involves activation of NF-kappaB in endothelial cells by fluid shear stress. Because this pathway involves integrins, we investigated the involvement of focal adhesion kinase (FAK). We found that FAK was not required for flow-stimulated translocation of the p65 NF-kappaB subunit to the nucleus but was essential for phosphorylation of p65 on serine 536 and induction of ICAM-1, an NF-kappaB-dependent gene. NF-kappaB activation by TNF-alpha or hydrogen peroxide was FAK independent. Events upstream of NF-kappaB, including integrin activation, Rac activation, reactive oxygen production, and degradation of IkappaB, were FAK independent. FAK therefore regulates NF-kappaB phosphorylation and transcriptional activity in response to flow by a novel mechanism.
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